| Background: Human cystatin C is a single non-glycosylated polypeptide chain consisting of 120 amino acid residues. Cystatin C widely exists in various body fluids, with constant concentration. The concentration of cystatin C in the circulation is not affected by gender, inflammation, and weight. Its concentration in the circulation is mainly determined by glomerular filtration rate. The production rate of cystatin C is constant. Cystatin C is freely filtered through by glomerular, and is not excreted and reabsorbed by nephric tubules.Heart failure is not an independent disease, but a terminal stage of all heart disease development. Heart failure has the irreversibility of development, high hospitalization rate, high mortality, high morbidity, huge health care consumption, and poor prognosis. Heart failure increasingly becomes a more serious problem in the world health care. The most common complication of chronic heart failure patients is chronic renal insufficiency or renal failure.Therefore, monitoring renal function is very important in heart failure management. The change of renal function is directly related to the clinical symptoms and subjective feeling of patients with heart failure. The glomerular filtration rate is the best method for measuring renal function. In clinical practice, the glomerular filtration rate measurement is a very complicated process. Because the inulin can be filtered through by glomerular, and is not reabsorbed or excreted by renal tubule and collecting duct, inulin is considered as the best exogenous substance of estimated glomerular filtration rate. Therefore, the clearance of inulin becomes the gold standard for measuring glomerular filtration rate, and often is used to evaluate the accuracy of other testing methods. In clinical practice, endogenous creatinine clearance is the most commonly used method of estimated glomerular filtration rate. Forthe evaluation of renal function, cystatin C is similar with serum creatinine, or even better than the latter. Some studies demonstrated that compared with creatinine-based glomerular filtration rate equation, cystatin C is more valuable on risk stratification and evaluating prognosis of heart failure.However, non-renal factors, i.e. drugs, may dramatically affect its levels in the circulation.Objective: The aim of this study was to evaluate the effect of corticosteroid treatment on serum cystatin C concentration in patients with symptomatic heart failure. At the same time, we analyzed the correlation between serum cystatin C and glomerular filtration rate after the glucocorticoid treatment in decompensated heart failure.Methods: We recruited fifty-six symptomatic heart failure patients, and recorded their general clinical status, including demographic data, the primary disease, hematology, urine samples, clinical drug treatment, etc. All patients were treated with prednisone. The median dose prednisone was 30 mg/d(the minimum dose was 15 mg/d; maximum dose was 60 mg/d). The treatment period is about two weeks. Concentrations of serum cystatin C and serum creatinine were recorded at baseline, and after about 2 weeks of treatment. At the same time, we record other biochemical indicator, including hematology indexes: blood routine, blood glucose, blood urea, serum sodium, serum potassium, serum chlorine, blood uric acid, blood hypersensitive C-reactive protein, blood renin, plasma angiotensin II, plasma aldosterone, brain natriuretic peptide(BNP), 24-hour urine volume, 24-hour urinary creatinine,24-hour urinary uric acid content of urine, 24-hour urinary sodium. We used twenty-four hour urinary creatinine to directly calculate glomerular filtration rate. Then glomerular filtration rate, fractional excretion of sodium, and urine flow rate were calculated using the following equations: glomerular filtration rate =(urinary creatinine concentration × 24-hour urine volume) /(serum creatinine concentration × 24 × 60 minutes). Glomerular filtration rate was then standardized by body surface area and expressed with mL/min/1.73m~2.Fractional excretion of sodium =(24-hour urine sodium × serum creatinineconcentration) /(serum sodium concentration × 24-hour urine creatinine) ×100. Urine flow rate = 24-hour urine volume /(24 × 60 minutes).Results: Prednisone treatment significantly increased serum cystatin C concentration from 1.24 ± 0.40 mg/L at baseline to 1.61 ± 0.80 mg/L at the end of study(P < 0.05). However, the elevation in serum cystatin C concentration was not associated with renal function impairment. Prednisone not only significantly decreased serum creatinine concentrations from 89.66 ±28.63 μmol/L at baseline to 76.55 ± 20.80 μmol/L after prednisone treatment(P < 0.05), but also significantly increased fractional excretion of sodium and urine flow rate. The data also showed there was a slight and but nonstatistically significant increase in glomerular filtration rate in such patients after prednisone treatment.Conclusions: Important non-renal factors, such as corticosteroids, can influence cystatin C concentration. Thus, it needs to be considered when interpreting cystatin C values in patients with heart failure receiving corticosteroid therapy. |
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